HIV infected patients are at the same, or even greater, risk for developing inflammatory arthritis. However, the nature of their chronic infection and increased susceptibility to opportunistic infection have prompted most clinicians to avoid using TNF inhibitors in this patients population, even in settings in which their use would otherwise be appropriate, since only a few case reports have been published detailing treatment experiences. Here, Cepeda et al (Ann Rheum Dis; published online 13 Dec 2007) report treatment outcomes in 8 HIV infected patients treated with TNF inhibitors.
Patient characterisitics and clinical outcomes were assessed via chart review in 8 HIV infected patients treated with TNF inhibitors in the setting of active rheumatic disease refractory to NSAIDs and non-biologic DMARDs. Patients underwent standard anti-tuberculosis screening prior to initiation of TNF inhibitor therapy. Of note, clinical practice dictated that therapy was not initiated in patients with a CD4 count below 200 or a viral load greater than 60,000 copies.
The mean follow-up time was 28 months, with a range of 2.5 to 55 months. Five patients were receiving antiviral therapy at the time of initiation of TNF inhibitors. Etanercept was started in all patients, but changes to infliximab or adalimumab were subsequently used in four patients due to inefficacy of initial etanercept. Only one patient was classifiable as having clinical AIDS.
TNF inhibitor therapy did not affect HIV viral load or CD4 count in seven of the patients followed. One patient had a rise in HIV viral load after initiation of infliximab that did not recur with subsequent infusions. No cases of tuberculosis or other opportunistic infections were noted. One patient, the only one of the 8 with clinical AIDS, developed a facial abscess while receiving infliximab that was treated with antibiotics. This patient had a baseline CD4 count of 268, the lowest of the 8 patients, and had been treated with methylprednisolone over 20 mg per day. In addition, one patient developed new onset iritis while treated with etanercept.
Six patients had excellent clinical responses to initial treatment. Both of the remaining patients had partial responses. Psoriasis appeared particularly sensitive to TNF inhibitor therapy. In general, corticosteroid therapy was able to be reduced or discontinued.
TNF inhibitor therapy may be safe and effective in HIV infected patients.
Chronic viral infections, such as the viral hepatitides and HIV, present a particular challenge to rheumatologists who must balance the need to treat the signs and symptoms of inflammatory arthritis with concerns that therapy may adversely affect immune homeostasis. This is especially true in the HIV infected patient, in whom concerns of a host of opportunistic infections also play into therapeutic decision making. Although the small number of patients included in this case series preclude making strong conclusions, there is some suggestion that these agents can be used safely in carefully chosen patients. The finding that the subject with the lowest baseline CD4 count was the one who developed a serious infection suggests that CD4 count may be useful in determining which HIV infected patients are appropriate for TNF inhibitor therapy. However, additional data from larger cohorts will be required to determine the appropriate cutoff levels.
Certain inflammatory syndromes, such as the seronegative spondyloarthropathies, are more frequent in HIV infected patients. Importantly, it should be noted that the efficacy of TNF inhibition has not been proven for these conditions in this subset of patients.